Fluoxetine is Neuroprotective in Early Brain Injury via its Anti-inflammatory and Anti-apoptotic Effects in a Rat Experimental Subarachnoid Hemorrhage Model.
10.1007/s12264-018-0232-8
- Author:
Hui-Min HU
1
;
Bin LI
2
;
Xiao-Dong WANG
1
;
Yun-Shan GUO
1
;
Hua HUI
1
;
Hai-Ping ZHANG
1
;
Biao WANG
1
;
Da-Geng HUANG
1
;
Ding-Jun HAO
3
Author Information
1. Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, 710054, China.
2. Key Laboratory of Resource Biology and Biotechnology in Western China (Ministry of Education), Northwest University, Xi'an, 710054, China.
3. Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, 710054, China. dochaodingjun@163.com.
- Publication Type:Journal Article
- Keywords:
Blood-brain barrier;
Fluoxetine;
Microglial activation;
Neuronal apoptosis;
Subarachnoid hemorrhage
- MeSH:
Animals;
Apoptosis;
drug effects;
Blood-Brain Barrier;
drug effects;
Brain Edema;
drug therapy;
etiology;
Cytokines;
genetics;
metabolism;
Disease Models, Animal;
Fluoxetine;
pharmacology;
therapeutic use;
In Situ Nick-End Labeling;
Male;
Neuroprotective Agents;
pharmacology;
therapeutic use;
Pain Measurement;
Psychomotor Performance;
drug effects;
RNA, Messenger;
metabolism;
Rats;
Rats, Sprague-Dawley;
Subarachnoid Hemorrhage;
complications;
drug therapy;
pathology;
Time Factors;
Vasospasm, Intracranial;
drug therapy;
etiology
- From:Neuroscience Bulletin
2018;34(6):951-962
- CountryChina
- Language:English
-
Abstract:
Fluoxetine, an anti-depressant drug, has recently been shown to provide neuroprotection in central nervous system injury, but its roles in subarachnoid hemorrhage (SAH) remain unclear. In this study, we aimed to evaluate whether fluoxetine attenuates early brain injury (EBI) after SAH. We demonstrated that intraperitoneal injection of fluoxetine (10 mg/kg per day) significantly attenuated brain edema and blood-brain barrier (BBB) disruption, microglial activation, and neuronal apoptosis in EBI after experimental SAH, as evidenced by the reduction of brain water content and Evans blue dye extravasation, prevention of disruption of the tight junction proteins zonula occludens-1, claudin-5, and occludin, a decrease of cells staining positive for Iba-1, ED-1, and TUNEL and a decline in IL-1β, IL-6, TNF-α, MDA, 3-nitrotyrosine, and 8-OHDG levels. Moreover, fluoxetine significantly improved the neurological deficits of EBI and long-term sensorimotor behavioral deficits following SAH in a rat model. These results indicated that fluoxetine has a neuroprotective effect after experimental SAH.
